Basic Science Orthobullets/Millers Book Flashcards
Overview of anticoagulation
What does Aspirin do and how does it work?
Introduction:
thromboxane function
under normal conditions thromboxane is responsible for the aggregation of platelets that form blood clots
prostaglandins function prostaglandins are local hormones produced in the body and have diverse effects including
the transmission of pain information to the brain
modulation of the hypothalamic thermostat
inflammation
Mechanism of ASA inhibits the production of prostaglandins and thromboxanes through irreversible inactivation of the cyclooxygenase enzyme within platelets
acts as an acetylating agent where an acetyl group is covalently and irreversibly attached to a serine residue in the active site of the cyclooxygenase enzyme.
this differentiates aspirin different from other NSAIDs which are reversible inhibitors
Metabolism
renal
Unfractionated Heparin (SQ)
Mechanism
binds and enhances ability of antithrombin III to inhibit factors IIa, III, Xa
Reversal
protamine sulfate
Metabolism
hepatic
Risk
bleeding
HIT (heparin induced thrombocytopenia)
EnoXAparen
Lovenox
Overview
molecular name: enoxaparin
trade name: Lovenox, Clexane
has advantage of not requiring lab value monitoring
Mechanism
LMWH acts in several sites of the coagulation cascade, with its principal action being inhibition of factor Xa
reversed by protamine sulfate
Metabolism
renal
Risk
bleeding
FondaParinux
Arixtra
Overview
trade name: Arixtra
has advantage of not requiring lab value monitoring
Mechanism
indirect factor Xa inhibitor (acts through antithrombin III)
Metabolism
renal
Evidence
studies show decreased incidence of DVT when compared to enoxaparin in hip fx and TKA patients
Risk highest bleeding complications
not to be used in conjunction with epidurals
Warfarin
Coumadin
Mechanism of anticoagulation inhibits vitamin K 2,3-epoxide reductase
prevents reduction of vitamin K epoxide back to active vitamin K
vitamin K is needed for gamma-carboxylation of glutamic acid for factorsII (prothrombin), VII (first affected), IX, X protein C, protein S
Monitoring
target level of INR (international normalized ratio) is 2-3 for orthopaedic patients
not achieved for 3 days after initiation
Reversal
vitamin K (takes up to 3 days)
fresh frozen plasma (acts immediately)
Risk
difficult to dose requires the frequent need for INR lab monitoring
can have adverse reaction with other drugs including
rifampin
phenobarbital
diuretics
cholestyramine
RIvaroXABAN
XArelto
Overview
others in the same class include apixaban (Eliquis) and edoxaban (Savaysa or Lixiana)
mechanism of action of these drugs can be deduced from the name.
Rivaro(Identifier)-xa(FactorXa)-ban(inhibitor)
Mechanism
direct Xa inhibitor
Metabolism
liver
Antidote
no current antidote- why you have to wait with surgery
andexanet alpha being investigated
Risk
bleeding
Half-life
8-hours (12-hours for apixaban)
urgent surgical procedures delayed until half-life spanned from last dose
Diabigatran
Pradaxa
Mechanism
reversible direct thrombin (factor IIa) inhibitor
Metabolism
renal
Antidote
idarucizumab (FDA approved Oct 2015)
Risk
GI upset
bleeding
Transexamanic Acid
TXA
synthethic lysine
Overview
an antifibrinolytic that promotes and stabilizes clot formation
studies have shown that TXA reduce perioperative blood loss and transfusion in THA and TKA
Mechanism
synthetic derivative of the amino acid lysine
competitively inhibits the activation of plasminogen by binding to the lysine binding site
at high concentrations, is a non-competitive inhibitor of plasmin
has roughly 8-10 times the antifibrinolytic activity of ε-aminocaproic acid
Dosing intravenous
10-20 mg/kg initial bolus dose followed by repeated doses of the initial TXA dose every 3 hours for 1-4 doses
10-20mg initial bolus followed either by an infusion of 1-10 mg/kg/hr for 4-30 hours
topical application is as effective as IV
sprayed onto open wound at completion of procedure
no detectable TXA in the bloodstream after topical application
Metabolism
<5% of the drug is metabolized
biological half-life in joint fluid is 3h, present in tissues for up to 17h
Risks
systematic review shows no increase in thromboembolic events
relatively few adverse reactions have been reported in the arthroplasty literature
**Tranexamic acid (TXA) works through the competitive inhibition of plasminogen activation.
TXA (Lysteda) is an antifibrinolytic that promotes and stabilizes clot formation. It competitively inhibits the activation of plasminogen by binding to the lysine binding site. TXA is effective in reducing the need for blood transfusions while not increasing the risk of VTE and renal complications. However, it is still advised that patients with cardiac stents and previous thromboembolic events including ischemic stroke not be administered TXA.**
Herbal supplements that affect bleeding:
Increased bleeding
gingko, ginseng, and garlic have been found to increase the rate of bleeding
related to effect on platelets
proper history taking can avoid complications
Increased warfarin effect (increase INR)omega-3 fish oil
affects platelet aggregation and vitamin K dependent coagulation factors
Reduced warfarin effect (reduces INR)
coenzyme Q10
green tea
direct warfarin antagonist (reduces INR)
St John’s wort
increases catabolism of warfarin (reduces INR)
where do Anticoagulants act on the clotting cascade?
what are the criteria vis MSIS for an infected periprosthethic joint?
What are the mechanism of actions for heparin, aspirin, warfarin, rivoxaban, dabigatran
the big Atran–
Warfarin inhibits vitamin K 2,3-epoxide reductase, thereby limiting the production of vitamin K-dependent clotting factors (II, VII, IX, X) as well as Protein C and Protein S.
Aspirin inhibits the production of prostaglandins and thromboxanes through irreversible inhibition of cyclooxygenase (COX, 1 and 2) and thus inhibits platelet aggregation.
Rivaroxaban is a direct inhibitor of factor Xa.
Dabigatran is a direct thrombin inhibitor.
Describe Transaminic Acid:
Factor Ia is fibrin. The enzyme that breaks down fibrin is plasmin. Tranexamic acid (TXA) is an antifibrinolytic that prevents the activation of plasmin from the inactive zymogen plasminogen.
Tranexamic acid competitively inhibits the activation of plasminogen to plasmin by binding to specific sites on both plasminogen and plasmin. Tranexamic acid has roughly eight times the antifibrinolytic activity of an older analogue, e-aminocaproic acid. It is used during joint replacement surgery to reduce blood loss and the need for transfusion.
Watts et al. review strategies for minimizing blood loss and transfusion. They recommend 1g of TXA prior to incision, and 1g at wound closure. They also recommend giving fluids for symptoms of anemia, rather than transfusion, as even high risk patients do well with sufficient intravascular volume even with low hemoglobin levels.
what are the half-lives of anticoagulation medications as it relates to surgery?
Warfarin, which is dosed daily, can take 72 to 96 hours to reach therapeutic levels. It has a plasma half-life of 36 to 42 hours. Low-molecular heparins have a plasma half-life of 4 to 5 hours, and fondaparinux has a half-life of 17 to 21 hours. Warfarin will not affect the International Normalized Ratio (INR) until 2 to 3 days after it is given. Patients on chronic warfarin therapy should have treatment stopped 3 to 5 days before elective surgery to allow the INR to normalize.
Xarelto is 8-12 hours. have to hold urgent surgery for those on it.
What herbal supplements affect platelets
Ginko
Garlic
Ginseng
The three G’s
what is the clotting cascade’s final product?
Thrombin–
converts soluble fibrinogen to insoluable fibrin
Review the genetic components of hypercoagulability:
List the risk factors for thromboembolic disease:
what are the recommendations on preventing VTE on arthroplasty?
Miller’s brief review of pharmacologic treatment for SVT prophylaxis:
Pharmacologic prophylaxis:
Surgical Care Improvement Project (SCIP) quality measures require DVT prophylaxis.
Aspirin
Irreversibly binds and inactivates COX in platelets, thereby reducing thromboxane A2
Weakest: Use of IPCD encouraged
Low bleeding risk: Should be considered for patients at higher risk for bleeding.
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Warfarin (Coumadin)
Prevents vitamin K γ-carboxylation in liver
Inhibits factors II, VII, IX, X, and proteins C and S
Vitamin K and fresh frozen plasma can reverse
Multiple reactions with drugs and diet
Must be monitored with international normalized ratio (INR; goal, 2–3)
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Heparin
Activates antithrombin III (ATIII), which then inactivates factor Xa and thrombin
Protamine sulfate can reverse
Short half-life: 2 hours
High bleeding rate in arthroplasty
Binds platelets—heparin-induced thrombocytopenia
Low-molecular-weight heparin (LMWH)
Reversibly inhibits factor Xa through ATIII and factor II
Protamine sulfate can reverse•
No monitoring needed
Less heparin-induced thrombocytopenia
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Higher risk for bleeding than with warfarin
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Fondaparinux (akin to oral heparin)
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Irreversibly but indirectly inhibits factor X through ATIII
Synthetic pentasaccharide
No monitoring
No antidote
Higher risk for bleeding than with LMWH
Rivaroxaban
Direct Xa inhibitor
Oral drug
Higher risk for bleeding than with LMWH
Hirudin
Direct thrombin (IIa) inhibitor
Intramuscular and oral (dabigatran) versions
No antidote
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Inferior vena cava (IVC) filter use: controversial
Should be considered in following conditions:
Contraindication to prophylaxis
Cerebral bleed/trauma
Spine surgery
Prior complication of prophylaxis
How do you assess cardiac risk factors prior to surgery?
American College of Cardiology/American Heart Association (ACC/AHA) elements for assessing risk
Clinical risk factors in perioperative cardiac risk
Major predictors
Unstable/severe angina, recent MI (<6 weeks)
Worsening or new-onset CHF
Arrhythmias
Atrioventricular (AV) block
Symptomatic ventricular dysrhythmia: bradycardia (<30 beats/min), tachycardia (>100 beats/min)
Severe aortic stenosis or symptomatic mitral stenosis
Other
Prior ischemic heart disease
Prior CHF
Prior stroke/TIA
Diabetes
Renal insufficiency (creatine >2 mg/dL)
Functional exercise capacity—measured in metabolic equivalents (METs) MET: 3.5 mL O2 uptake/kg/min
Perioperative risk elevated if unable to meet 4-MET demand
Walk up flight of steps or hill (= 4 METs)
Heavy work around house (>4 METs)
Can patient walk four blocks or climb two flights of stairs?
Please quantify surgery specific risks by procedure:
Surgery-specific risk:
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High risk (>5% risk of death/MI)
Aortic, major or peripheral vascular procedures
Intermediate risk (1%–5% risk of death/MI)
Orthopaedic, ENT, abdominal/thoracic or procedures
Low risk (<1% risk of death/MI)—usually do not need further clearance
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Ambulatory surgery, endoscopic or superficial procedures
What are cardiac recommendations prior to surgery?
Twelve-lead ECG if:
CAD and intermediate-risk procedure
One clinical risk factor and intermediate-risk procedure
Noninvasive evaluation of left ventricular function if:
—Three or more clinical risk factors and intermediate- risk procedure
—Dyspnea of unknown origin
—CHF with worsening dyspnea without testing in 12 months
β-Blockers and statins should be continued around the time of surgery.
Acetylsalicylic acid (ASA) should be stopped 7 days prior to surgery.
Cardiology consultation should be considered for patients taking other agents (clopidogrel, prasugrel).
Risk of stent thrombosis balanced with that of surgical bleed
What are measures of shock recovery?
Lactate—indirect marker of tissue hypoperfusion
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Best measures of adequate resuscitation:
Clinical measure of organ function: urine output more than 30 mL/h
Laboratory measure: serum lactate less than 2.5 mg/dL
Review the types of shock and their clinical presentation:
Neurogenic shock
High spinal cord injury (also anesthetic accidents)
Loss of sympathetic tone and of vasomotor tone of peripheral arterial bed
Bradycardia, hypotension, warm extremities
Treatment: vasoconstrictors and volume
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Septic shock (vasogenic)
Number one cause of ICU death
Mortality 50%
Bacterial toxins stimulate cytokine storm.
Examples: gram-negative lipopolysaccharides, toxic shock superantigen
Inflammatory mediators cause endothelial dysfunction and peripheral vasodilation
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Treatment:
Identification and treatment of infections
Prompt resection of dead tissue
Appropriate antibiotics
Cardiogenic shock
Bad pump: Extensive MI, arrhythmias
Blocked pump (obstructive shock)
Massive “saddle” pulmonary embolism
Tension pneumothorax
Cardiac tamponade
Beck triad: hypotension, muffled heart sounds,
neck vein distension
Pulsus paradoxus
Decreased systolic BP with inspiration
Treatment: pericardiocentesis
Hypovolemic shock:
Most common shock of trauma
Volume loss from bleeds or burns
“Third spacing” also a cause
Neuroendocrine response: save heart and brain
Peripheral vasoconstriction
BP may be normal
Pale, cold, clammy extremities
Percentage of blood loss key to symptoms/signs:
Class I: up to 15% blood volume loss
Vital signs can be maintained.
Pulse below 100 beats/min
Class II: 15%–30% blood volume loss
Tachycardia (>100 beats/min), orthostatic,
Anxious
Increased diastolic BP
Class III: 30%–40% blood volume loss
Decreased systolic BP
Oliguria
Confusion, mental status changes
Class IV: more than 40% blood volume loss
Life threatening; patient is obtunded
Narrowed pulse pressure
IImmeasurable diastolic BP
Treatment
First, ABCs of resuscitation: then, bleeding must be stopped.
Blood products make better resuscitation fluids than saline.
How to address perioperative pulmonary issues around surgery:
Higher in cases that involve thorax such as scoliosis
Highest in patients with prior disease
Spinal/epidural anesthesia favored over general
Medical treatment should be maximized around surgery.
Symptomatic COPD: anticholinergic inhalers (ipratropium; May require corticosteroids
Asthma
Presence of wheezes or shortness of breath: β-agonist inhalers (albuterol)
Perioperative oral steroids safe
Systemic glucocorticoid should be considered if forced expiratory volume in 1 minute (FEV1) or peak expiratory flow rate (PEFR) is below 80% predicted values/personal best.
Postoperative atelectasis
Like the associated cough, the workup is usually nonproductive.
Deep breathing/incentive spirometry—equally effective
Postoperative pneumonia takes up to 5 days to manifest.
Productive cough, fever/chills, increased WBC count
Radiograph: pulmonary infiltrates
Smoking cessation improves outcomes
Patients should stop 6–8 weeks preoperatively.
Nicotine supplements do no harm to wound.
Fewer pulmonary complications
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Smokers have six times more pulmonary complications.
Fewer wound healing issues and wound infections
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Lower nonunion rate
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Shoulder, neck, and thoracic pain in smokers
Prompts careful evaluation of lung fields
Superior sulcus tumor (Pancoast tumor)
Intrinsic atrophy of hand—C8–T1
Describe ARDS:
Pulmonary failure due to edema (see Fig. 1.56A)
Pathophysiology
Complement pathway activated
Increased pulmonary capillary permeability
Intravascular fluid floods alveoli
Results
Hypoxia, pulmonary HTN
Right heart failure
50% mortality
Etiology
Blunt chest trauma, aspiration, pneumonia, sepsis
Shock, burns, smoke inhalation, near drowning
Orthopaedic: Long-bone trauma
Clinical symptoms
Tachypnea, dyspnea, hypoxia, decreased lung compliance
Pao2/fio2 ratio below 200
Imaging:
Radiographs: diffuse bilateral infiltrates, “snowstorm”
CT: ground glass appearance
Treatment: Aggressive supportive care
Prompt diagnosis and treatment of musculoskeletal infections:Prompt treatment of long-bone fractures
Ventilation with positive end-expiratory pressure (PEEP)
100% O2
Describe Fat Emboli Syndrome:
Petechial rash: fat to skin
Neurologic symptoms: fat to brain
Mental status changes: confusion, stupor
Rigidity, convulsions, coma
Pulmonary collapse: fat showers lung
ARDS: hypoxia, tachypnea, dyspnea
Associated with long-bone fractures
Characterize the common blood disoders as it relates to surgery:
Common inherited bleeding disorders:
Vonwillebrands disease AD (Vonwillebrands factor)
Hemophilia Ax-linked recessive
Hemophilia B. Christmas
Von Willebrand disease: autosomal dominant
Most common genetic coagulation disorder
Von Willebrand factor dysfunction
Binds platelets to endothelium
Carrier for factor VIII
Treatment: desmopressin
Hemophilia A (VIII): X-linked recessive
Hemophilia B (IX) Christmas disease: X-linked recessive
List some medications that should be stopped prior to surgery:
Platelet-inhibitor drugs (aspirin, clopidogrel, prasugrel, NSAIDs)
Drugs that cause thrombocytopenia
Penicillin, quinine, heparin, LMWH
Anticoagulants (see earlier discussion on DVT)
Supplements
Fish oil, omega-3 fatty acids, vitamin E
Garlic, ginger, Ginkgo biloba
Review Tourniquet technique
Tourniquets: tissue effect relates to time and pressure
Used no longer than 2 hours
Time to restoration of equilibrium
5 minutes after 90 minutes of use
15 minutes after 3 hours
Prolonged use can cause tissue damage.
Nerve damage compressive (not ischemic)
Electromyography: subclinical abnormalities in 70% with routine use
Slight increase in pain
Wider tourniquets distribute forces
Pad underneath prevents skin blisters in TKA
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Lowest pressure needed for effect should be used
100–150 mm Hg above systolic BP
200 mm Hg upper extremity
250 mm Hg lower extremity
Ways to manage surgical bleeding:
Tranexamic acid
Synthetic lysine analogue; acts on fibrinolytic system
Competitive inhibitor of plasminogen activation
Reduces blood loss with no increase in DVT.
Temperature
Mild hypothermia increases bleeding time and blood loss.
•
Intraoperative “cell saver” may be cost-effective if:
About 1000 mL of blood loss is expected
Recovery of 1 or more unit of blood is anticipated.
Techniques not yet found to be effective or cost-effective
Bipolar sealant, topical sealants, autologous donation
Reinfusion systems, routine transfusions over 8 g/dL Hb
Preoperative techniques to address anemia
Oral iron 30–45 days preoperatively
Vitamin C increases iron absorbtion
Folate and vitamin B12 deficiency also a source of anemia
Erythropoietin if preoperative Hb below 13
Review the risks and benefits of blood transfusion
Transfusions
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Ratio of 1:1:1 blood product resuscitation is superior to saline fluid
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Preoperative Hb most significant predictor of need
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Various guidelines for when to transfuse
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Hb less than 6 g/dL: transfusion
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Hb 7–8 g/dL: transfusion of postoperative patients
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Hb 8–10 g/dL: transfusion of symptomatic patients
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Restrictive transfusion strategies
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Lower 30-day mortality trend
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Lower infection risk trend
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Greatest benefits to orthopaedic patients
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No difference in functional recovery
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Transfusions risks
•
Leading risk: transfusion of wrong blood to patient
•
Occurs in 1 in 10,000 to 1 in 20,000 RBC units transfused
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Transfusion reactions
Febrile nonhemolytic transfusion reaction
Most common
1–6 hours post-transfusion
From leukocyte cytokines released from stored cells
Leukoreduction decreases incidence
Acute hemolytic transfusion reaction
Medical emergency
ABO incompatibility
IgM anti-A and anti-B, which fix complement
Rapid intravascular hemolysis
Classic triad: fever, flank pain, red/brown urine (rare)
Can cause disseminated intravascular coagulation (DIC), shock, and acute renal failure (ARF) due to acute tubular necrosis (ATN)
Positive direct antiglobulin (Coombs) test result
Delayed hemolytic transfusion reactions
Reexposure to previous antigen (i.e., Rh or Kidd)
History of pregnancy, prior transfusion, transplantation
3–30 days post-transfusion
Anemia, mild elevation of unconjugated bilirubin, spherocytosis
Anaphylactic reactions: about 1 in 20,000
Rapid hypotension, angioedema
Shock, respiratory distress
Frequently involve anti-IgA and IgE antibodies
Treatment: cessation of transfusions, ABCs of resuscitation, epinephrine
Urticarial reactions: about 1%–3%
Mast cell/basophils release of histamine—hives
Infectious risks
Bacterial: 0.2 per million packed red blood cell (PRBC) units transfused
Gram-positive organisms
Cryophilic organisms: Yersinia, Pseudomonas
HTLV—approximately 1 in 2 million
HIV—approximately 1 in 2 million
Hepatitis C—approximately 1 in 2 million
Hepatitis B—approximately 1 in 250,000
Review the Liver issues with surgery:
Liver failure: critical for producing proteins and metabolizing toxins
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Laboratory findings
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Increased aspartate aminotransferase (AST), alanine aminotransferase (ALT), and bilirubin
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INR above 1.5, low platelets (<150,000 cells/μL)
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Acute—most commonly viral and drug induced
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Acetaminophen—number one cause in United States
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Other toxins: alcohol, occupational, mushrooms
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Viral hepatitis
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Chronic—cirrhosis is end-stage fibrosis of liver
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Common: hepatitis (B, C), alcoholism, hemochromatosis
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Classifications can be helpful to estimate risks
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Child classification—most widely used
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Based on laboratory results and physical examination
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Model for End-Stage Liver Disease (MELD) score (http://www.mayoclinic.org/medical-professionals/model-end-stage-liver-disease/meld-model)
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Formula based on bilirubin, INR, creatinine
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Studies highlight mortality at 90 days relative to MELD score
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<9: about 2% mortality
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10–19: about 6% mortality
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20–29: about 20% mortality
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30–39: about 53% mortality
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>40: about 71% mortality
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Complication rates from surgery are extremely high.
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In patients undergoing arthroplasty, MELD score above 10 predicted
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Three times the complication rate
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Four times the rate death
What is Ogilvee’s syndrome?
Large bowel dilation
•
Abdominal distension the prominent symptom
•
Colonic perforation should be avoided.
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Risk factors
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Elderly or male patient
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Previous bowel surgery
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Diabetes, hypothyroidism
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Electrolyte disorders
Radiographic findings
Distended transverse and descending colon and cecum (see Fig. 1.58C)
Colonic diameter more than 10 cm risks perforation.
Treatment
Nothing by mouth status
Neostigmine
Colonic decompression
Review pseudomembraneous collitis
Most common antibiotic-associated colitis
Change in colon flora favors Clostridium difficile
Makes enterotoxin-A and cytotoxin-B
Many antibiotics
Clindamycin, fluoroquinolones
Penicillins and cephalosporins
Can become severe fulminant colitis
Toxic megacolon and perforations
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Risk factors
Elderly hospitalized patient
Severe illness
Antibiotic use
Proton pump inhibitor use
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Diagnosis
Watery diarrhea with fever
Leukocytosis, lower abdominal pain
Laboratory findings
WBC count more than 15,000 cells/μL
Stool specimen should be tested for C. difficile toxin
PCR or ELISA
KUB (kidney, ureter, bladder) (plain abdominal) radiograph
Toxic megacolon: greater than 7 cm
Thumbprinting (see Fig. 1.58D)
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Treatment
Oral metronidazole
Oral vancomycin (IV will not work)
Fidaxomicin
Colectomy if unresponsive and severe
Megacolon, WBC count more than 20,000 cells/μL
What are the surgical considerations for obstructive sleep apnea?
Intermittent hypercapnia and hypoxia
Decreased CO2-induced respiratory drive
Extreme sensitivity to opioids
Leads to
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Pulmonary HTN
Cardiac arrhythmias
GERD (reflux) directly related to BMI
Delayed gastric emptying
Increased risks for aspiration/intubation
Higher risk for complications (2–4 times greater)
Respiratory failure, ICU transfers, increased length of stay
Increased postoperative O2 desaturation
Increased intubation, aspiration pneumonia, ARDS
Increased MI, arrhythmias (atrial fibrillation)
Screening tools: STOP-BANG (Fig. 1.59)
- Snoring, tired, observed apnea, pressure (HTN)
- BMI over 35, age older than 50 years, neck
circumference larger than 40 cm, gender male
Five or more factors present—high risk of
severe OSA
Best practices
Initiation or continuation of CPAP use
More than 2 weeks of preoperative CPAP
improved HTN, O2 saturation, apneic events
Pulmonary HTN: in 20%–40% of patients with
OSA
Preoperative serum bicarbonate predicts
hypoxia in OSA
Chronic respiratory acidosis
Site of service (American Society of Anesthesiology consensus statement)
Ambulatory surgery under local/regional—lower
risk
Avoid procedures requiring opioids—greater
risk
Comorbid conditions must be optimized for outpatient surgery. HTN, arrhythmias, CHF, cardiovascular disease, and metabolic syndrome.
Metabolic syndrome = obesity, hypertension, hypercholesterolemia, dyslipidemia, and insulin resistance
Avoidance of flat supine position; sitting position opens airway.
Review Malignant hyperthermia:
Autosomal dominant genetic defect of T-tubule of sarcoplasmic reticulum
Ryanodine receptor defect (RYR1)
Dihydropyridine receptors (DHP)
Triggered by volatile anesthetics and succinylcholine
Creates an uncontrolled release of Ca2+
Sustained muscular contraction (masseter rigidity)
Increased end-tidal CO2
Earliest and most sensitive sign
Mixed respiratory and metabolic alkalosis
Hyperthermia is classic but occurs later.
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Muscle damage
Myoglobin from rhabdomyolysis can cause ARF.
Elevated creatine kinase
Hyperkalemia can lead to ventricular arrhythmias.
Treatment with dantrolene
Decreases intracellular Ca2+
Stabilizes sarcoplasmic reticulum
Treatment of high serum potassium
Hydration
Cooling
what are some radiation safety concerns for the orthopedic surgeon?
Should be considered for every fluoroscopic case
Increased radiation exposure associated with
–Imaging of larger body parts
–Positioning the extremity closer to the x-source
–Use of large C-arm rather than mini C-arm
Factors to decrease the amount of radiation exposure
–Minimizing exposure time
–Using collimation to manipulate the x-ray beam
–Use of protective shielding
–Maximizing the distance between the surgeon and
the radiation beam
–Utilizing mini C-arm whenever feasible (associated
with minimal radiation exposure)
–Surgeon control of the C-arm
What are contraindications to MRI?
Contraindications
Pacemakers
Cerebral aneurysm clips
Shrapnel or hardware, in certain locations
MRI Imaging Terminology
Review of clinically relevant nuclear medicine studies:
EMG interpretations:
Key Highlights of NCS:
Evaluation of peripheral nerves
Nerve impulses stimulated and recorded by surface electrodes
Allows calculation of conduction velocity
Measures latency (time from stimulus onset to response) and response amplitude
Late responses (F wave, H reflex) allow evaluation of proximal lesions.
Impulse travels to the spinal cord and returns
